CGRP has seen resurgence in headlines lately, not so much because it is a brand new discovery, but because of the anxious hope Migraineurs have for a new in class medicine that might be helpful to them.

Not much is known about what starts a Migraine attack and what happens during the attack, which is why we seem to be in a stalemate research-wise. We do know a little something about CGRP’s role in the process however, so researchers are talking about and using what they know for now to more precisely target our Migraines for better treatments.

CGRP is not easy to explain, but here are some basics…

CGRP stands for Calcitonin Gene-Related Peptide.

It is an amino acid peptide produced by neurons in our bodies and which has been implicated in Migraine pathogenesis – the process of how a Migraine happens in our bodies.

The type of CGRP protein that researchers are currently looking at seems to have only one job: Pain.

Our brains themselves do not have the capacity to feel pain. However, it is currently thought that during a Migraine attack, sensory neurons in the trigeminal nerves (the nerves inside our head that are responsible for feeling and pain in the head and face) are activated and release CGRP.

CGRP binds to special receptors that switch on (activate) and cause many of the symptoms of Migraine including vasodilation, inflammation and pain.

During Migraine, CGRP can be found in plasma taken from the jugular vein as well as saliva.

Giving and IV of CGRP triggers Migraine in Migraineurs.

Triptans work in part by increasing the amount of calcium inside cells, which then seems to decrease CGRP.

OnabotulinumtoxinA (Botox) is believed to work to prevent release of CGRP.

All of this is information we have known for a while. There is more we haven’t yet been quite able to put to use. Because CGRP itself isn’t the end of the story, it is helpful to explain how CGRP works in its receptors. It is these receptors researchers have been looking at particularly closely.